Objective:To investigate the protective mechanism of N-acetylcysteine(NAC) in ischemia-reperfusion injury of spinal cord. Methods:Forty-five New England rabbits were randomly assigned to one of the 3 groups:sham-operation group(n=5);ischemic reperfusion group:animals were given 0.9% NaCl before operation,which were divided into 4 sub-groups:ischemia 30 minutes/reperfusion 30 minutes group(group A,n=5),ischemia 30 minutes/reperfusion 2 hours group(group B,n=5) and ischemia 30 minutes/reperfusion 8 hours group (group C,n=5),ischemia 30 minutes/reperfusion 24 hours group (group D,n=5);lNAC group:animals were given NAC before operation,and sub-groups are exactly the same as the ischemic reperfusion group. The morphology of spinal cord was observed by hematoxylin and eosin(HE)staining and electron microscope. The phosphorylation of JNK(p-JNK) were detected by western blot. Results:①In the ischemic reperfusion group,the apoptosis of neurocytes of spinal cord in group B were detected by electronmicroscope. In NAC group,the apoptosis of neurocytes of spinal cord was detected in group D. ②In the ischemic reperfusion group,JNK was activated in group B,and enhanced with the ischemia time increasing. In NAC group,JNK was activated in group D,and the activities were lower than the corresponding group in the ischemic reperfusion group. Simultaneously JNK protein expression were not significantly different between two groups. Conclusion:Ischemia-reperfusion could cause the injuries of spinal cord by activating JNK(the MRPKs family ). Giving NAC before ischemia could protect neurocytes from JNK-mediated apoptosis induced by severe ischemia reperfusion injury.